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Objective@#To investigate the causes of disease among patients with liver disease hospitalized in Department of Infectious Diseases in our hospital and the changes in such causes within the past 20 years.@*Methods@#A retrospective analysis was performed for the clinical data of 7570 patients who were admitted to our hospital from January 1995 to December 2015. The chi-square test was used for the statistical analysis of constituent ratio.@*Results@#Of all 7570 patients with liver disease, 4930 (65.13%) had viral hepatitis, 332 (4.39%) had immune disease, 215 (2.84%) had drug-induced liver injury, 192 (2.54%) had fatty liver disease, 88 (1.16%) had schistosome-induced liver disease, 160 (2.11%) had inherited metabolic diseases, and 20 (0.13%) had vascular disease; 689 (9.1%) still had no clear cause of disease at discharge. The proportion of patients with viral hepatitis was 77.61% in the first 10 years and 59.19% in the last 10 years (P < 0.01). As for liver disease caused by hepatotropic virus, there were significant increases in the proportion of patients with hepatitis C or hepatitis E from the first to the last 10 years (hepatitis C: 2.24% vs 15.56%, P < 0.01; hepatitis E: 18.61% vs 23.07%, P < 0.05), while there were significant reductions in the proportion of patients with hepatitis B (68.14% vs 60.01%, P < 0.05) or hepatitis A (10.7% vs 1.36%, P < 0.05). The proportion of patients with immune diseases was 0.82% in the first 10 years and 6.08% in the last 10 years (P < 0.01). There were also certain changes in the proportion of patients with liver disease caused by other reasons.@*Conclusion@#There is a large proportion of patients with viral hepatitis among patients with liver disease hospitalized in Department of Infectious Diseases in a large general hospital, especially hepatitis B and E caused by hepatotropic virus. There is a certain change in the epidemiology of liver disease within the past 20 years, with a reduction in the proportion of patients with viral hepatitis and an increase in the proportion of patients with non-infectious liver diseases. There is a large proportion of patients with unknown causes of liver disease.
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The noninvasive measurement of liver stiffness (LS) was evaluated by transient elastography (FibroScan) and the possible influencing factors from the patients' clinical situations including age, gender, liver inflammation represented by alanine transaminase (ALT) and total billirubin (TBIL) level, HBV replication (HBV DNA loads), portal vein pressure (portal vessel diameter, PVD), splenic thickness (SPT) and body mass index (BMI) were analyzed in patients with chronic hepatitis B (CHB). A total of 466 patients including 31 patients with acute-on-chronic liver failure (ACLF), and 435 patients with chronic hepatitis B (CHB) among which 82 patients were diagnosed with liver cirrhosis (LC) by clinical manifestations and liver B-type ultrasonic inspection were enrolled at Tongji Hospital from April to December 2009. LS was measured by a FibroScan device (EchoSens, France). Simultaneously, ALT and TBIL levels, HBV DNA loads, PVD, SPT and BMI in all patients were also tested. Forty-one healthy volunteers served as controls. The values of LS were correlated positively with ages of CHB patients and significantly higher in males than in females. In patients with BMI>28 kg/m(2) (obesity) and abnormal levels of ALT and TBIL, LS values were significantly increased as compared with those having normal levels of ALT and TBIL. The patients with ACLF had the highest LS value. Furthermore, LS values in the patients with LC were significantly higher than those in patients without LC. It is concluded that noninvasive measurement of liver fibrosis by FibroScan provides an alternative method to evaluate liver fibrosis of patients with CHB. In order to properly illustrate the stiffness value taken by transient elastography, patients' gender should be taken into consideration and it is also suggested to avoid possible influencing factors including liver inflammation (high levels of ALT and TBIL) and obesity (high BMI).
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OBJECTIVE@#To improve the diagnosis and treatment of Kimura's disease (KD) by investigating its clinical characteristics, pathological features and complications.@*METHOD@#The clinical data of 33 cases of KD were analyzed retrospectively.@*RESULT@#Of 33 cases, 22 showed the mass on head and neck, while in the other cases, the mass distributed in the region of groin, axillary fossa, hilum of lung and mesentery. Regional lymph nodes were involved in 21 cases and major salivary glands were invaded in 8 cases. Twenty-three cases had typical peripheral eosinophilia, although only in 2 patients the quantity of serum total IgE increased markedly. Urine abnormalities happened to 7 cases, such as massive proteinuria (3 cases) and hematuria (2 cases). Among 6 cases which underwent bone marrow aspiration, 2 showed eosinophilia. Two cases were complicated with nephritic syndrome. Six cases were combined with local inflammation on head and neck and 2 cases were combined with malignant tumor.@*CONCLUSION@#Mass on the head and neck is the typical clinical manifestation in KD, with regional lymph nodes and major salivary glands involved most. Serum total IgE and histopathologic examination should always be done to confirm KD, especially in the cases with unknown eosinophilia increasing.
Subject(s)
Adolescent , Adult , Aged , Child , Female , Humans , Male , Middle Aged , Young Adult , Angiolymphoid Hyperplasia with Eosinophilia , Diagnosis , Pathology , Therapeutics , Head , Pathology , Immunoglobulin E , Blood , Lymph Nodes , Pathology , Neck , Pathology , Retrospective Studies , Salivary Glands , PathologyABSTRACT
To study the effect of HBx gene on the apoptosis of the cell lines (L02, HepG2) and the interaction between HBx and X-linked inhibitor of apoptosis protein (XIAP), the apoptosis of pcDNA3.1-HBx transiently transfected cell lines (L02, HepG2) was detected by flow cytometry and the mRNA expression of XIAP was assayed by real-time RT-PCR. Our study showed (1) the morphology of L02/pcDNA3.1-HBx was changed and the appearance of the cells mimicked that of HepG2 cells; (2) HBx gene could be detected in L02/pcDNA3.1-HBx and HepG2/ pcDNA3.1-HBx; (3) the apoptosis rate of L02/pcDNA 3.1-HBx was higher than that of L02 cells (P<0.01) and the apoptosis rate of HepG2/pcDNA3.1-HBx was lower than that of HepG2 cells (P<0.05); (4) the XIAP expression in L02 was about 3 times that in L02/pcDNA3.1-HBx cells (P<0.01), and the expression of XIAP in HepG2/pcDNA3.1-HBx was about 4 times that in HepG2 (P<0.01). It is concluded that HBx gene may promote the apoptosis of normal hepatocytes and inhibit the apoptosis of cells of hepatic carcinoma by regulating the expression of XIAP.
ABSTRACT
To study the effect of HBx gene on the apoptosis of the cell lines (L02, HepG2) and the interaction between HBx and X-linked inhibitor of apoptosis protein (XIAP), the apoptosis of pcDNA3.1-HBx transiently transfected cell lines (L02, HepG2) was detected by flow cytometry and the mRNA expression of XIAP was assayed by real-time RT-PCR. Our study showed (1) the morphology of L02/pcDNA3. 1-HBx was changed and the appearance of the cells mimicked that of HepG2 cells; (2) HBx gene could be detected in L02/pcDNA3.1-HBx and HepG2/pcDNA3.1-HBx;(3) the apoptosis rate of L02/pcDNA 3.1-HBx was higher than that of L02 cells (P＜0.01) and the apoptosis rate of HepG2/pcDNA3. 1-HBx was lower than that of HepG2 cells (P＜0.05); (4) the XIAP expression in L02 was about 3 times that in L02/pcDNA3.1-HBx cells (P＜0.01), and the expression of XIAP in HepG2/pcDNA3. 1-HBx was about 4 times that in HepG2 (P＜0.01). It is concluded that HBx gene may promote the apoptosis of normal hepatocytes and inhibit the apoptosis of cells of hepatic carcinoma by regulating the expression of XIAP.
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Objective:To observe the effect of Shuganlidanpaishiwan and its different extractive fractions on gallbladder motility of rabbits. Methods:Establishing 100 rabbit animal models,the rabbits were randomly divided into 10 groups:the low and high dose groups of Shuganlidanpaishiwan,methanolic extract,petroleum ether and ethylacetate,negative and positive control groups,to observe the gallbladder motility of every group of animals. Results:The contraction rate of gallbladder on 30th minute after Adm were(9.40?3.36) ,(10.00?2.00) ,(14.00?2.00) on high dose of Shuganlidanpaishiwan group,methanolice extract group and the low dose of petroleum ether group respectively,which were significantly higher than that of control group. Conclusion:Shuganlidanpaishiwan,methanolice extract and petroleum ether extract could improve the gallbladder contractility.
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The gene and the amino acid sequence of the structural and regulatory region of the Pseudomonas aeruginosa with different resistance patterns were analyzed. Six strains with different resistance patterns were selected and the AmpC beta-lactamase was identified. The objective gene fragment was amplified by colonies PCR. The sequences of the PCR-products were analyzed. The DNA sequence of the structural gene ampC and the regulatory genes ampR, ampD and ampE was detected. The 6 strains and the wild-type Pseudomonas aeruginosa are highly homogeneous in structural and regulatory region. Some new mutant points were found.
Subject(s)
Bacterial Proteins/genetics , DNA, Bacterial/genetics , Point Mutation/genetics , Pseudomonas aeruginosa/enzymology , Pseudomonas aeruginosa/genetics , Sequence Analysis, DNA , beta-Lactam Resistance/genetics , beta-Lactamases/geneticsABSTRACT
The gene and the amino acid sequence of the structural and regulatory region of the Pseudomonas aeruginosa with different resistance patterns were analyzed. Six strains with different resistance patterns were selected and the AmpC β-lactamase was identified. The objective gene fragment was amplified by colonies PCR. The sequences of the PCR-products were analyzed. The DNA sequence of the structural gene ampC and the regulatory genes ampR, ampD and ampE was detected. The 6 strains and the wild-type Pseudomonas aeruginosa are highly homogeneous in structural and regulatory region. Some new mutant points were found.
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To study the resistant mechanism and clinical significance of pseudomonas aeruginosa to beta-lactam antibiotics, the outer membrane permeability rate of 30 P. aeruginosa strains to 5 beta-lactam antibiotics was measured and their production of beta-lactamase and the beta-lactamase genes they carried detected. Furthermore, the relationship between the permeability, beta-lactamase and the clinical effects of beta-lactam antibiotics was observed. By using 14C-penicillin and liquid-scintillant isotope assay, the affinity of penicillin binding proteins (PBPS) was measured and their roles in the resistant mechanism studied. It was revealed that the permeability rate was higher in sensitive strains than in resistant ones (P < 0.05). All strains harbored 1-4 beta-lactamase genes and produced beta-lactamase. Higher permeability rate and higher degree of stability to beta-lactamase indicated better clinical therapeutic effects. The affinity of PBPs changed little without regard to the permeability and beta-lactamase. These results suggested that the permeability of outer membrane and beta-lactamase, but not PBPs, played important roles in the resistant mechanism of P. aeruginosa to beta-lactam antibiotics and affected the clinical therapeutic effectiveness of some patients.
Subject(s)
Anti-Bacterial Agents/pharmacology , Bacterial Outer Membrane Proteins/metabolism , Microbial Sensitivity Tests , Permeability , Pseudomonas aeruginosa/drug effects , beta-Lactam Resistance/genetics , beta-Lactamases/metabolism , beta-Lactams/pharmacologyABSTRACT
To study the resistant mechanism and clinical significance of pseudomonas aeruginosa to beta-lactam antibiotics, the outer membrane permeability rate of 30 P. aeruginosa strains to 5 beta-lactam antibiotics was measured and their production of beta-lactamase and the beta-lactamase genes they carried detected. Furthermore, the relationship between the permeability, beta-lactamase and the clinical effects of beta-lactam antibiotics was observed. By using 14C-penicillin and liquid-scintillant isotope assay, the affinity of penicillin binding proteins (PBPS) was measured and their roles in the resistant mechanism studied. It was revealed that the permeability rate was higher in sensitive strains than in resistant ones (P < 0.05). All strains harbored 1-4 beta-lactamase genes and produced beta-lactamase. Higher permeability rate and higher degree of stability to beta-lactamase indicated better clinical therapeutic effects. The affinity of PBPs changed little without regard to the permeability and beta-lactamase. These results suggested that the permeability of outer membrane and beta-lactamase, but not PBPs, played important roles in the resistant mechanism of P. aeruginosa to beta-lactam antibiotics and affected the clinical therapeutic effectiveness of some patients.
Subject(s)
Humans , Anti-Bacterial Agents , Pharmacology , Bacterial Outer Membrane Proteins , Metabolism , Microbial Sensitivity Tests , Permeability , Pseudomonas aeruginosa , beta-Lactam Resistance , Genetics , beta-Lactamases , Metabolism , beta-Lactams , PharmacologyABSTRACT
Objective To explore the potential of converting the chloramphenicol resistant clinical E. Coli isolates to chloramphenicol sensitive ones by employing external guide sequence(EGS) technique in vitro. Methods Recombinant plasmids with EGScat 1+2 and tetracycline resistant gene, named PAlterl EGScat1+2, was constructed. Routine Cacl 2 method was used to introduce recombinant plasmid into the chloramphenicol resistant clinical isolates E. Coli 4758. Colony PCR was used to test and A600 was used to detect growth rates in liquid and solid culture of various concentrations of chloramphenicol. Results The chloramphenicol resistant clinical isolates E. Coli 4758 grew well in chloramphenicol(35 ?g/ml, 70 ?g/ml, 105 ?g/ml, 170 ?g/ml) plates whereas the transformants tE4758 with PAlter1 EGScat 1+2 failed to grow in these concentrations, which indicated its resistance to the chloramphenicol was reversed. Conclusions EGS molecules are able to convert the drug resistance in clinical E. Coli isolates in vitro.